Water pipe smoking and human oral cancers

Medical Hypotheses 74 (2010) 457–459

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Water pipe smoking and human oral cancers Samer Rastam a,b, Fu-Min Li c, Fouad M. Fouad a, Haysam M. Al Kamal a, Nizar Akil a,b, Ala-Eddin Al Moustafa a,b,d,e,* a

Syrian Research Cancer Centre, Syrian Society Against Cancer, Aleppo, Syria Departments of Anatomy & Embryology and Pathology, Aleppo University, Aleppo, Syria c Emergency Medical Centre, Xu Zhou Hospital, South-East University, Xu Zhou, Jiang Su, China d Department of Oncology, McGill University, Montreal, Quebec, Canada e Department of Mechanical & Industrial Engineering, Concordia University, Montreal, Quebec, Canada b

a r t i c l e

i n f o

Article history: Received 27 September 2009 Accepted 4 October 2009

s u m m a r y While cigarette smoking is recognized as an important risk factor in human oral cancers, the effect of water pipe smoking (WPS) on these cancers is not known. WPS is very common in the young adult population, especially in the Middle East, and has been associated with several respiratory problems. However, to date, there have been no studies examining the association between WPS and the progression of human oral cancers. Currently, the role of WPS in human oral cancers remains uncertain because of the limited number of investigations. This raises the question of whether WPS plays a significant role in the development of human oral carcinomas. In this paper, we propose the hypothesis that human oral normal epithelial cells are vulnerable to persistent WPS; moreover, WPS could play an important role in the initiation of a neoplastic transformation of human normal oral epithelial cells. Therefore, we believe that an international collaboration of epidemiological and clinical studies as well as cellular and molecular biology investigations is necessary to answer this important question. Ó 2009 Elsevier Ltd. All rights reserved.

Introduction Cancers of the oral cavity, larynx and pharynx, collectively referred to as squamous cell carcinomas of the head and neck are estimated by the WHO to be the eighth most common cancer worldwide. More than 290,000 new cases worldwide are being diagnosed annually with oral squamous cell carcinomas [1]. Surgery, radiation and/or chemotherapy have not improved the 50% overall 5-year survival of this devastating disease over the past 25 years [2,3]. In general, the incidence of these cancers has significant local variation and is increasing in some parts of the world [1]. For example, in India and other Asian countries including some of the Middle East counties, oral and oropharyngeal malignancies are very high in comparison with other regions in the world, with this particularly high prevalence being attributed to the influence of carcinogens and region-specific epidemiological factors, especially tobacco including water pipe smoking (WPS), betel quid chewing and viruses such as high-risk HPVs and EBV [4–10]. WPS is traditional and common in different parts of the world especially in the majority Middle East countries and some North

* Corresponding author. Address: Syrian Research Cancer Centre, Syrian Society Against Cancer, Aleppo, Syria. Tel.: +963 21 2644246; fax: +963 21 26499150. E-mail addresses: [email protected], aalmoust@encs. concordia.ca, [email protected] (A.-E. Al Moustafa). 0306-9877/$ - see front matter Ó 2009 Elsevier Ltd. All rights reserved. doi:10.1016/j.mehy.2009.10.013

African countries as well as India [11–14]. It is believed to have been used to smoke tobacco or other substances by the indigenous people of Africa and Asia including Middle East for at least four centuries [12,13]. The water pipe is now the object of renewed interest, as its use has recently been spreading among young people in the western countries including the United States and Canada [14,15, and personal observation]. Though, a precise evaluation of the health effects of WPS is hindered by the paucity of published studies [14,16]. Smoke from water pipes contains most of the compounds that are also present in cigarette smoke, albeit in different proportions. More importantly, the longer duration of a WPS session leads to a much higher yield of tar, nicotine, carbon monoxide, polycyclic aromatic hydrocarbons and heavy metals than cigarette smoking. The water pipe smoker may therefore inhale the equivalent of 100 or more cigarettes [16–18]. Studies on the consequences for human health of WPS mostly come, for the time being, from the Middle East with occasional evaluations as part of case-control studies looking at risk factors for specific cancers that include the assessment of different forms of smoking, for example in India or China, where an increased risk of lung cancer was indicated as well as other cancers, such as lip and oral cancers [7,12–14,19]. Overall, these studies demonstrate that WPS could play an important role in human oral carcinogenesis. Meanwhile, the specific role of WPS in human oral carcinomas remains to be determined.

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Hypothesis In this paper, we propose the hypothesis that human normal oral epithelial cells are susceptible to WPS, a cultural activity that is very common among young adults, especially in the Middle East. Moreover, we presume that WPS enhances the progression of human oral cancers. Therefore, we firmly believe that extensive epidemiological, clinical and biological studies, including a microarray investigation, are required to elucidate the role of WPS in human oral carcinogenesis.

Discussion and conclusion It is well established that tobacco-induced pulmonary cellular network presents a unique environment in which carcinogenesis proceeds in complicity with surrounding lung inflammatory, structural and stromal cells [20,21]. The commonalities in smoking, chronic obstructive pulmonary disease (COPD) and lung cancer begin with the profound alterations induced by cigarette smoke and probably by WPS, which contains known carcinogens as well as high levels of reactive oxygen species (ROS) [20,22,23]. The ready induction of ROS after tobacco smoke exposure leads to impairment of epithelial and endothelial cell functions as well as inflammation. The ongoing inflammatory processes in COPD may be persistent even after smoking cessation and have been quantified and related to disease progression [20,23]. As COPD progresses, the percentage of the airways that contain macrophages, neutrophils, T and B cells as well as lymphoid aggregates containing follicles increases [20,21,23]. Smoking-induced epithelial abnormalities can serve both as targets for abnormal inflammatory responses and as initiators of deregulated inflammation. Cytokines chemokines and growth factors released by alveolar macrophages, lymphocytes, neutrophils, endothelial cells and fibroblasts can act to promote epithelial dysfunction and malignant progression [20,21,24]. Some of these relationships are most clearly demonstrable in genetically engineered animal models [25]. Epithelial cells can also serve as a site of deregulated inflammatory responses in pulmonary tumorigenesis. For example, chronic exposure to tobacco compounds can lead to loss of p53 and K-ras mutation. These in turn can lead to deregulated inflammation and angiogenesis. For example, Komarova et al. [26] found that p53, by acting to suppress NF-kB activity, could serve as a ‘‘buffer” for inflammatory responses. These studies clearly demonstrate the carcinogenic role of cigarette smoke and probably WPS in human lung and oral epithelial cells. On the other hand, it is well known that water pipe smokers inhale the equivalent of 100 or more cigarettes which can affect the lungs and the oral cavity of the smokers [16–18]. Therefore, we firmly believe that WPS can provoke lung cancer as well as oral cancer. However, an international collaboration of epidemiological and clinical studies as well as cellular and molecular biology including microarray investigations are necessary to elucidate the specific role of WPS in human cancers especially oral cancer. For example in our laboratory, we have previously identified a list of genes that are differentially expressed between matched primary human oral normal and cancer cells using microarray technology. Our list of genes represents a useful source of potential targets for human oral cancers prevention and/or therapeutics [27]. Accordingly, we think that identification of differential gene deregulation patterns between human normal oral epithelial cells and their matched counterpart exposed to the water pipe smoke is the basis for a comprehensive understanding of the molecular mechanism of the carcinogenic process related to WPS, as these differences will most likely represent the coordinated alteration of critical pathways involved in human oral carcinogenesis of water pipe smokers.

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